clinical trials

# Aging, Senescence, and Glaucoma Glaucoma is a leading cause of blindness and its risk rises with age. In aged eyes, cells can enter a **senescent** state – they stop dividing but stay alive – and release harmful signals called the *senescence-associated secretory phenotype* (SASP). Senescent cells in the eye can worsen disease. For example, aged trabecular meshwork cells (the filter in front of the eye) become stiff and clogged, raising eye pressure ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC12155388/#:~:text=senescence,86)). In the retina and optic nerve, senescent cells release cytokines (like IL-6, IL-8, IL-1β) and enzymes (MMPs) that cause inflammation, tissue remodeling, and nerve cell death ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC10917531/#:~:text=indicating%20a%20direct%20influence%20of,22%20%2C%20%2074)) ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC11375756/#:~:text=reactive%20oxygen%20species,24%7D%20and)). These SASP factors have been found in human glaucomatous eyes and animal models of eye pressure, where they drive retinal ganglion cell (RGC) damage ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC10917531/#:~:text=indicating%20a%20direct%20influence%20of,22%20%2C%20%2074)) ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC6996954/#:~:text=Experimental%20ocular%20hypertension%20induces%20senescence,IOP)). Targeting these cells is a new idea: removing or quieting them may help protect the optic nerve. # Senescence in the Eye Senescent cells build up in key eye tissues. In the **trabecular meshwork (TM)**, senescence stiffens the meshwork and increases resistance to fluid outflow ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC12155388/#:~:text=senescence,86)). This raises intraocular pressure, a main risk factor for glaucoma. In humans with glaucoma, more senescent TM cells (marked by enzymes like SA-β-gal, or proteins p16^INK4a and p21^CIP1) have been measured compared to normal eyes ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC10917531/#:~:text=Patients%20with%20glaucoma%20exhibit%20a,expression%20of%20miRNAs%20is%20related)). High p16 and p21 in TM cells correlate with glaucoma and fewer TM cells survive into old age ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC10917531/#:~:text=Patients%20with%20glaucoma%20exhibit%20a,expression%20of%20miRNAs%20is%20related)). In the **optic nerve head and retina**, aging and stress cause RGCs and supporting cells (astrocytes, microglia) to become senescent. These cells then secrete SASP factors – pro-inflammatory cytokines (IL-6, IL-1β, IL-8), chemokines (CCL2, CXCL5), and matrix metalloproteinases – which poison nearby neurons and propagate senescence to neighbors ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC10917531/#:~:text=indicating%20a%20direct%20influence%20of,22%20%2C%20%2074)) ([pmc.ncbi.nlm.nih.gov](https://

clinical trials

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